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Bacillary dysentery as a causative factor of irritable bowel syndrome and its pathogenesis
Open accessAbstract
Background and aims: The incidence of irritable bowel syndrome (IBS) or functional bowel disorders (FBD) after bacillary dysentery (BD) has not been extensively evaluated, and little is known of the pathogenesis of post-infective (PI) IBS. Therefore, we investigated the incidence of IBS and FBD in a Chinese patient population who had recovered from BD. To further elucidate its pathogenesis, neuroimmunological changes, including interleukins (IL), mast cells, neuropeptides, and the relationship between mast cells and intestinal nerves, were investigated. Methods: A cohort study of 295 patients who had recovered from BD (shigella identified from stool in 71.4%) and 243 control subjects consisting of patient siblings or spouses who had not been infected with BD were included in the study. All subjects were followed up using questionnaires for 1–2 years to explore the incidence of FBD and IBS, as defined by the Rome II criteria. In 56 cases of IBS (PI and non-PI) from another source, the number of mast cells in biopsy specimens from the intestinal mucosa were stained with antitryptase antibody and counted under light microscopy. Also, the relationship of mast cells to neurone specific enolase (NSE), substance P (SP), 5-hydroxytryptamine (5-HT), or calcitonin gene related peptide positive nerve fibres was observed using double staining with alcian blue and neuropeptide antibodies. In 30 cases of IBS (PI-IBS, n = 15) taken at random from the 56 cases, expression of interleukin (IL)-1α, IL-1β, and IL-1 receptor antagonist (IL-1ra) mRNAs in intestinal mucosa were identified using reverse transcription-polymerase chain reaction. The above results were compared with 12 non-IBS controls. Results: In the BD infected cohort, the incidences of FBD and IBS were 22.4% and 8.1% (in total)–10.2% (among those in who shigella were identified) respectively, which were significantly higher (p<0.01) than the incidences of FBD (7.4%) and IBS (0.8%) in the control cohort. A longer duration of diarrhoea (⩾7 days) was associated with a higher risk of developing FBD (odds ratio 3.49 (95% confidence interval 1.71–7.13)). Expression of IL-1β mRNA in terminal ileum and rectosigmoid mucosa was significantly higher in PI-IBS patients (p<0.01). The number of mast cells in the terminal ileum mucosa in PI-IBS (11.19 (2.83)) and non-PI-IBS patients (10.78 (1.23)) was significantly increased compared with that (6.05 (0.51)) in control subjects (p<0.01). Also, in the terminal ileum and rectosigmoid mucosa of IBS patients, the density of NSE, SP, and 5-HT positively stained nerve fibres increased (p<0.05) and appeared in clusters, surrounding an increased number of mast cells (p<0.01 compared with controls). Conclusions: BD is a causative factor in PI-IBS. The immune and nervous system may both play important roles in the pathogenesis of PI-IBS.
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“Several studies have demonstrated increased concentrations of activated mast cells in patients with IBS compared with controls (11, 13, 24, 46, 89, 94, 121, 187).”
From Intestinal microbiota and immune function in the pathogenesis of irritable bowel syndrome (2013) · cites this paper as [187]
In the citing paper
“Notably, some studies demonstrated an increase in activated mast cells in biopsies from specific regions of the GI tract (i.e., cecum and terminal ileum) but not from other regions (e.g., ascending colon, descending colon, rectum) (89, 121, 187), whereas other studies have found activated mast cells in the descending colon (11, 13).”
From Intestinal microbiota and immune function in the pathogenesis of irritable bowel syndrome (2013) · cites this paper as [187]
In the citing paper
“Levels of interleukin (IL)-1β mRNA may be increased in the small intestine, colon, and rectum of patients with PI-IBS compared with healthy controls (75, 187), supporting the hypothesis that low-grade inflammation is present in patients with PI-IBS.”
From Intestinal microbiota and immune function in the pathogenesis of irritable bowel syndrome (2013) · cites this paper as [187]
In the citing paper
“The importance of the interaction between the intestinal microbiota and immune system in IBS patients is demonstrated by a few studies in patients with PI-IBS, indicating activation of the GI immune system following the acute GI infection (57, 58, 75, 89, 94, 124, 168, 170, 187)”
From Intestinal microbiota and immune function in the pathogenesis of irritable bowel syndrome (2013) · cites this paper as [187]
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Metadata
- Authors
- Wang, L.-H., Fang, X.-C., & Pan, G.-Z.
- Affiliations
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Corresponding author
- Pan, G-Z
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2004-07-09
- Volume
- 53
- Issue
- 8
- Pages
- 1096-1101
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- PMC
- PMC1774156
- OpenAlex
- W2158018898
- Cited by
- 387
- References
- 51
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 3 · 2023: 8 · 2022: 3 · 2021: 9 · 2020: 10 · 2019: 17 · 2018: 17 · 2017: 18 · 2016: 19 · 2015: 19 · 2014: 31 · 2013: 18 · 2012: 23
- FWCI
- 19.91
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- other-oa
- Locations
- Gut (publishedVersion, other-oa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
- Keywords
- shigellosis, irritable bowel syndrome, functional bowel disorders, Shigella, mast cells, neuroimmunology, substance P, calcitonin gene-related peptide, serotonin, interleukin-1, interleukin-1 receptor antagonist, intestinal nerves, pathogenesis, diarrhea duration
- MeSH terms
- Adult, Colonic Diseases, Functional, Diarrhea, Dysentery, Bacillary, Female, Follow-Up Studies, Humans, Interleukin-1, Intestinal Mucosa, Male, Mast Cells, Nerve Fibers, Phosphopyruvate Hydratase, Risk Factors, Serotonin, Substance P, Calcitonin Gene-Related Peptide, Irritable Bowel Syndrome
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